ArticlemedRxiv : the preprint server for health sciences2026
Workplace Pollution and Risk of Incident Coronary Artery Disease.
Article in medRxiv : the preprint server for health sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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Authors and funding
11 authors.
Funding
Abstract
Importance: Genetic factors only explain ~50% of an individual's lifetime CAD risk. Workplace pollution exposure likely represents a significant, under-recognized, and modifiable contributor. Clarifying its independent effect - distinct from residential air pollution - could inform targeted prevention, clinical risk assessment, and policy strategies. Objective: To quantify the independent association between workplace pollution exposure and incident CAD, rigorously adjusting for canonical risk factors, genetic risk, socioeconomic deprivation index, and residential air pollution. Design Setting and Participants: A prospective cohort analysis of 103,599 adults in the UK Biobank with complete baseline employment history and specialized workplace environment surveys. Participants with prior CAD, or missing genetic information, canonical risk factor data, or residential air pollution measurements, were excluded. Exposure: Cumulative, self-reported duration of exposure to workplace pollutants (including dust, smoke, exhaust, chemicals, asbestos, paints, and pesticides), summarized as a percentile measure. Main Outcomes and Measures: Incident CAD. Associations were estimated using Cox proportional hazards models adjusted for demographics, comorbidities, CAD polygenic risk score, and residential air pollution metrics, accounting for competing death events. Results: The cohort (median age 64 years; 43% male) had high baseline prevalence of smoking (41%) and co-morbidities (hypertension 27%, hyperlipidemia 16%, diabetes 4.3%). Common exposures included smoke (56%), dust (39%), and chemicals (27%). Over a median 7.5-year follow-up, 4,327 CAD cases occurred. Compared to the low exposure group, high workplace pollution exposures showed a stronger unadjusted association with CAD (hazard ratio [HR], 1.51; 95% CI, 1.40-1.63) relative to residential air pollution (unadjusted HR, 1.23; 95% CI, 1.14-1.33). Importantly, in multivariable models, workplace pollution remained independently associated with higher CAD incidence (adjusted HR, 1.21; 95% CI, 1.03-1.41), robust to all adjustment. Significant specific drivers included paints, thinners or glues, diesel exhaust, fumes, asbestos, and dust. Conclusions and Relevance: Workplace pollution is confirmed as a robust, independent risk factor for incident CAD. Its association is demonstrably stronger than residential air pollution and persists despite comprehensive adjustment for genetic predisposition and traditional cardiovascular risk factors. These findings underscore the need to strengthen worker protections, integrate occupational history into clinical risk assessment, and prioritize mechanistic research into non-lipid pollution pathways.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.